Anatomy of the bacitracin resistance network in Bacillus subtilis

Publication type:
Journal article
Metadata:
Autoren
  • Jara Radeck
  • Susanne Gebhard
  • Peter Shevlin Orchard
  • Marion Kirchner
  • Stephanie Bauer
  • Thorsten Mascher
  • Georg Fritz
Autoren-URL
https://www.webofscience.com/api/gateway?GWVersion=2&SrcApp=fis-test-1&SrcAuth=WosAPI&KeyUT=WOS:000379684200003&DestLinkType=FullRecord&DestApp=WOS_CPL
DOI
10.1111/mmi.13336
eISSN
1365-2958
Externe Identifier
  • Clarivate Analytics Document Solution ID: DR1SC
  • PubMed Identifier: 26815905
ISSN
0950-382X
Ausgabe der Veröffentlichung
4
Zeitschrift
MOLECULAR MICROBIOLOGY
Paginierung
607 - 620
Datum der Veröffentlichung
2016
Status
Published
Titel
Anatomy of the bacitracin resistance network in <i>Bacillus subtilis</i>
Sub types
  • Article
Ausgabe der Zeitschrift
100

Data source: Web of Science (Lite)

Other metadata sources:
Abstract
<jats:title>Summary</jats:title><jats:p>Protection against antimicrobial peptides (AMPs) often involves the parallel production of multiple, well‐characterized resistance determinants. So far, little is known about how these resistance modules interact and how they jointly protect the cell. Here, we studied the interdependence between different layers of the envelope stress response of <jats:italic>Bacillus subtilis</jats:italic> when challenged with the lipid II cycle‐inhibiting AMP bacitracin. The underlying regulatory network orchestrates the production of the ABC transporter BceAB, the UPP phosphatase BcrC and the phage‐shock proteins LiaIH. Our systems‐level analysis reveals a clear hierarchy, allowing us to discriminate between primary (BceAB) and secondary (BcrC and LiaIH) layers of bacitracin resistance. Deleting the primary layer provokes an enhanced induction of the secondary layer to partially compensate for this loss. This study reveals a direct role of LiaIH in bacitracin resistance, provides novel insights into the feedback regulation of the Lia system, and demonstrates a pivotal role of BcrC in maintaining cell wall homeostasis. The compensatory regulation within the bacitracin network can also explain how gene expression noise propagates between resistance layers. We suggest that this active redundancy in the bacitracin resistance network of <jats:italic>B. subtilis</jats:italic> is a general principle to be found in many bacterial antibiotic resistance networks.</jats:p>
Autoren
  • Jara Radeck
  • Susanne Gebhard
  • Peter Shevlin Orchard
  • Marion Kirchner
  • Stephanie Bauer
  • Thorsten Mascher
  • Georg Fritz
DOI
10.1111/mmi.13336
eISSN
1365-2958
ISSN
0950-382X
Ausgabe der Veröffentlichung
4
Zeitschrift
Molecular Microbiology
Sprache
en
Online publication date
2016
Paginierung
607 - 620
Datum der Veröffentlichung
2016
Status
Published
Herausgeber
Wiley
Herausgeber URL
http://dx.doi.org/10.1111/mmi.13336
Datum der Datenerfassung
2023
Titel
Anatomy of the bacitracin resistance network in <scp><i>B</i></scp><i>acillus subtilis</i>
Ausgabe der Zeitschrift
100

Data source: Crossref

Abstract
Protection against antimicrobial peptides (AMPs) often involves the parallel production of multiple, well-characterized resistance determinants. So far, little is known about how these resistance modules interact and how they jointly protect the cell. Here, we studied the interdependence between different layers of the envelope stress response of Bacillus subtilis when challenged with the lipid II cycle-inhibiting AMP bacitracin. The underlying regulatory network orchestrates the production of the ABC transporter BceAB, the UPP phosphatase BcrC and the phage-shock proteins LiaIH. Our systems-level analysis reveals a clear hierarchy, allowing us to discriminate between primary (BceAB) and secondary (BcrC and LiaIH) layers of bacitracin resistance. Deleting the primary layer provokes an enhanced induction of the secondary layer to partially compensate for this loss. This study reveals a direct role of LiaIH in bacitracin resistance, provides novel insights into the feedback regulation of the Lia system, and demonstrates a pivotal role of BcrC in maintaining cell wall homeostasis. The compensatory regulation within the bacitracin network can also explain how gene expression noise propagates between resistance layers. We suggest that this active redundancy in the bacitracin resistance network of B. subtilis is a general principle to be found in many bacterial antibiotic resistance networks.
Addresses
  • Technische Universität Dresden, Institute of Microbiology, Dresden, Germany.
Autoren
  • Jara Radeck
  • Susanne Gebhard
  • Peter Shevlin Orchard
  • Marion Kirchner
  • Stephanie Bauer
  • Thorsten Mascher
  • Georg Fritz
DOI
10.1111/mmi.13336
eISSN
1365-2958
Externe Identifier
  • PubMed Identifier: 26815905
Funding acknowledgements
  • DFG priority program SPP1617 ‘Phenotypic Heterogeneity and Sociobiology of Bacterial Populations’: FR 3673/1-2 to GF and MA 2837/3-2 to TM
Open access
false
ISSN
0950-382X
Ausgabe der Veröffentlichung
4
Zeitschrift
Molecular microbiology
Schlüsselwörter
  • Cell Wall
  • Bacillus subtilis
  • Bacitracin
  • Bacterial Proteins
  • Anti-Bacterial Agents
  • Drug Resistance, Bacterial
  • Signal Transduction
  • Gene Expression Regulation, Bacterial
Sprache
eng
Medium
Print-Electronic
Online publication date
2016
Paginierung
607 - 620
Datum der Veröffentlichung
2016
Status
Published
Datum der Datenerfassung
2016
Titel
Anatomy of the bacitracin resistance network in Bacillus subtilis.
Sub types
  • Research Support, Non-U.S. Gov't
  • Journal Article
Ausgabe der Zeitschrift
100

Data source: Europe PubMed Central

Abstract
Protection against antimicrobial peptides (AMPs) often involves the parallel production of multiple, well-characterized resistance determinants. So far, little is known about how these resistance modules interact and how they jointly protect the cell. Here, we studied the interdependence between different layers of the envelope stress response of Bacillus subtilis when challenged with the lipid II cycle-inhibiting AMP bacitracin. The underlying regulatory network orchestrates the production of the ABC transporter BceAB, the UPP phosphatase BcrC and the phage-shock proteins LiaIH. Our systems-level analysis reveals a clear hierarchy, allowing us to discriminate between primary (BceAB) and secondary (BcrC and LiaIH) layers of bacitracin resistance. Deleting the primary layer provokes an enhanced induction of the secondary layer to partially compensate for this loss. This study reveals a direct role of LiaIH in bacitracin resistance, provides novel insights into the feedback regulation of the Lia system, and demonstrates a pivotal role of BcrC in maintaining cell wall homeostasis. The compensatory regulation within the bacitracin network can also explain how gene expression noise propagates between resistance layers. We suggest that this active redundancy in the bacitracin resistance network of B. subtilis is a general principle to be found in many bacterial antibiotic resistance networks.
Date of acceptance
2016
Autoren
  • Jara Radeck
  • Susanne Gebhard
  • Peter Shevlin Orchard
  • Marion Kirchner
  • Stephanie Bauer
  • Thorsten Mascher
  • Georg Fritz
Autoren-URL
https://www.ncbi.nlm.nih.gov/pubmed/26815905
DOI
10.1111/mmi.13336
eISSN
1365-2958
Ausgabe der Veröffentlichung
4
Zeitschrift
Mol Microbiol
Schlüsselwörter
  • Anti-Bacterial Agents
  • Bacillus subtilis
  • Bacitracin
  • Bacterial Proteins
  • Cell Wall
  • Drug Resistance, Bacterial
  • Gene Expression Regulation, Bacterial
  • Signal Transduction
Sprache
eng
Country
England
Paginierung
607 - 620
Datum der Veröffentlichung
2016
Status
Published
Datum, an dem der Datensatz öffentlich gemacht wurde
2017
Titel
Anatomy of the bacitracin resistance network in Bacillus subtilis.
Sub types
  • Journal Article
  • Research Support, Non-U.S. Gov't
Ausgabe der Zeitschrift
100

Data source: PubMed

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